Abstract

The abnormal expression of miRNA-146a is related to the progression of coronary arteries. This study intends to explore the protective effect of miRNA-146a on vascular smooth muscle cells (VSMCs) after coronary intervention and the related mechanism. 10 miniature pigs were randomly assigned into control group, model group, blank group, miRNA-146a group, cilostazol group, and STAT3 signaling agonist group followed by analysis of the morphology and viability of VSMCs, expression of miRNA-146a, STAT3, NF-kB, TNF-a, IL-6, and AT-1R as well as the relationship between miR-146a and STAT3. The BNP (192.39±12.32) pg/ml and cTnI (14.20±2.12)μg/L of model group were significantly higher than those of control group (P< 0.05). miRNA-146a level was highest in miRNA-146a group and cilostazol group, while lower in other two groups with the lowest level in agonist group (P<0.05). The cell viability and AngII level of miRNA-146a group and cilostazol group were lower, and higher in the other two groups with highest level in pathway agonist group (P< 0.05). miRNA-146a group and cilostazol group showed lower expressions of STAT3, NF-kB, TNF-a, IL-6, AT-1R than the other two groups. The pathway agonist group showed significantly higher level than blank group (P<0.05). liposome nanoparticles carrying miRNA-146a inhibited the activity of STAT3 signaling, down-regulated the levels of downstream factors including TNF-a, IL-6, and TNF-a and subsequently decreased AngII and AT-1R levels, therefore playing a protective effect on VSMCs after coronary intervention.

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